Fig. 8From: METTL3 mediates Ang-II-induced cardiac hypertrophy through accelerating pri-miR-221/222 maturation in an m6A-dependent mannerGraphical abstract of the whole study. METTL3 in CMs was upregulated in response to Ang-II, promoting m6A modification on pri-miR-221/222, thus leading to increased miR-221/222 expression. Subsequently, DKK2 was inhibited and Wnt/β‐catenin/c-Myc pathway was activated, finally promoting myocardial hypertrophyBack to article page